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Unexpected sudden death after lateral medullary infarction
  1. Delta Medical Center, 1905 Harbert Avenue, Memphis, TN 38104, USA

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    I read with interest the study of Fitzek et al,1 which included 15 patients with lower brain stem infarction. One patient with a “complete Wallenberg's syndrome” (No 15) died during the period of observation. Details on that patient's death are not included in the paper.

    Through personal communication with the authors I have learned that their patient No 15, a 69 year old man, died unexpectedly 14 days after an acute brain stem infarction. Because the family refused a necropsy, we do not know with certainty whether some other acute process was involved in the patient's death. However, an ECG and chest radiograph after presentation had been normal.

    Recent reports2-5 have described patients who experienced unexpected sudden cardiorespiratory arrest several days after lateral medullary infarction, at a time when they were convalescing well and were stable medically and neurologically after a stroke which caused minimal motor disability. The reports have speculated about mechanisms by which cardiorespiratory arrest occurred; cardiac arrhythmia is among these.4

    Although I do not know many pertinent details surrounding the death of the 69 year old man described by Fitzek et al,1 I speculate that his death may have resulted from cardiopulmonary arrest caused by an intermediate event in which the lateral medullary infarction and surrounding brain tissue disturbance (possibly ischaemic penumbra) influenced brain stem cardiac and respiratory centres together with autonomic pathways in a manner which at this time is not understood.

    A recent neuropathological study6 of five patients disclosed similar characteristic ischaemic lesions in the solitary tract nuclei of the medulla after subacute hypoperfusion of the brain during acute heart failure. It was speculated that these medullary lesions had in turn caused autonomic instability which precipitated death in each case. It is plausible that ischaemic lesions of the solitary tract nuclei result initially with some lateral medullary infarctions, and that such lesions may in turn precipitate some occurrences of cardiorespiratory arrest.


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